UMEM Educational Pearls - Cardiology

The Unforgotten: ECG Utilization to Differentiate Athletic Heart vs. Brugada

- Highly trained athletes develop ECG changes as a physiologic consequence of increased vagal tone; The ECG manifestations of early repolarization (ER) can range from simple J–point elevation to anterior (V1 to V3) "domed" ST-segment elevation and negative T wave.

- The former raises problems of differential some forms of ER with the “ coved-type” pattern seen in Brugada Syndrome (BS).

- A recent study compared the ECG tracings of 61 athletes w/a “domed” ST-segment elevation & negative T wave and 92  age/sex-matched BS patients w/a “ coved-type” pattern to identify an ECG criteria for distinguishing benign athletic changes seen in ER from BS.

- ECG analysis focused on ST-segment elevation at J-point (STJ ) and at 80 milliseconds after J-point (ST80 ).

- Athletes had a lower maximum amplitude of STJ  (p < 0.001) & lower STJ /ST80 (p < 0.001)

- All patients (100%) with BS showed a downsloping ST-segment configuration (STJ/ST80 > 1) versus only 2 (3%) athletes (p < 0.001)

- An upsloping ST-segment configuration (STJ /ST80 < 1) showed a sensitivity of 97%, a specificity of 100%, and a diagnostic accuracy of 98.7% for the diagnosis of ER.

A: ER

B: Brugada 

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Posterior Myocardial Infarctions (PMI)

- Posterior myocardial infarctions (PMI) are different than typical ST-elevation MI; the ECG findings include: septal & anterior ST-segment depression, dominant tall/broad R waves, and upright T waves.

- In a study among 117,739 subjects with STEMI, 824 with PMI were more likely to present with cardiac arrest, cardiogenic shock, and congestive heart failure.

- The median time from arrival ECG to revascularization with PCI was longer among subjects with PMI.

- The median time from arrival ECG to systemic thrombolysis was also longer among subjects with a PMI.

- Increased awareness and recognition of PMI is needed to improve reperfusion times among this subpopulation with STEMI.

 

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Left Ventricular Hypertrophy & Arrhythmias: Any Association?

Associations between left ventricular hypertrophy (LVH) and both supraventricular (SVT)/ventricular arrhythmias (VT/VF) have previously been reported.

A recent review & meta-analysis of 10 studies (27,141 patients) revealed the following:

    - Incidence of SVT was 11% with LVH compared to 1% without (p <0.001)

    - LVH patients had 3.4-fold greater odds of developing SVT

    - Incidence of VT/VF was 5.5% with LVH compared to 1.2% without (p <0.001)

    - LVH patients has 2.8 greater odds of developing VT/VF

The reason for increased arrhythmogenicity in LVH is not clearly understood.

A consistently observed abnormality in LVH is non-uniform propagation of the action potential throughout the myocardium, which sets the stage for arrhythmias based on early or delayed afterdepolarizations.

Given the heterogeneity in this meta-analysis further research between LVH & sustained arrhythmias is needed to infer true causality.

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Title: APACHE-HF Scoring System

Category: Cardiology

Posted: 1/12/2015 by Semhar Tewelde, MD (Updated: 2/18/2025)
Click here to contact Semhar Tewelde, MD

APACHE-HF Scoring System

The Acute Physiology and Chronic Health Evaluation (APACHE) scoring system was established in the 1980's to predict critically ill patient prognosis (APACHE II, III, and IV have been published in last two decades).

The APACHE II scoring system involves combining 3 separate scores (acute physiology score, chronic health score, and age), which can be cumbersome to apply & thus is not often utilized in the emergency department (modified APACHE II doesn't include chronic health score & is less taxing).

No unique scoring system for acute heart failure (AHF) has been analyzed until present; the APACHE-HF score includes 8 criteria: mean arterial pressure (MAP), pulse, sodium, potassium, hematocrit, creatinine, age, and glasgow coma score (GCS).

AHF in-hospital mortality data was analyzed and compared using APACHE II, modified APACHE II, and APACHE- HF scores and the predictive value of the APACHE-HF score was found to be optimal when compared to the others.

 

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Holiday Heart 

- Holiday heart commonly refers to alcohol use and rhythm disturbances, particularly supraventricular tachydysrhythmias.

- The most common rhythm disorder is atrial fibrillation (AF), which usually converts to normal sinus rhythm within 24 hours and antiarrhythmic therapy is typically not indicated.

- Analyses of ECGs in patients who have consumed a large quantity of alcohol show prolongation of the PR, QRS, and QT intervals.

- 2014 AHA/ACC/HRS updated guidelines for nonvalvular AF utilize the CHA2DS2-VASc (congestive heart failure, hypertension, age ≥75 years [doubled], diabetes mellitus, prior stroke or TIA or thromboembolism [doubled], vascular disease, age 65 to 74 years, and sex category) score for assessment of stroke risk. 

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Title: Brugada Syndrome

Category: Cardiology

Keywords: Brugada (PubMed Search)

Posted: 12/21/2014 by Semhar Tewelde, MD (Updated: 1/19/2015)
Click here to contact Semhar Tewelde, MD

Brugada Syndrome

Brugada syndrome is an inherited arrhythmogenic channelopathy described by ST-segment elevation in the right precordial leads and an increased risk of sudden cardiac death.

There are 3 electrocardiographic patterns:

Type 1 – Coved morphology w/ST-elevation >2 mm, followed by a negative T wave in at least 1 right precordial lead

Type 2 - Saddleback morphology w/ST-elevation >2mm, with a positive or biphasic T wave

Type 3 - Either coved, or saddleback morphology with <2mm ST-elevation

Type 1 pattern is often underestimated because of its sporadic/fluctuating appearance on ECG, which can be either spontaneously occurring or drug-induced (drug-induced variant has a more favorable prognosis).

Fever has been a well-documented culprit in unmasking Brugada pattern by increasing the sodium channel dysfunction & accelerating the late sodium current inactivation.

A recent study in a large population of patients with type 1 Brugada attempted to identify other patterns unmasking Brugada using 24-hour holter monitoring. * There is now evidence that there is a higher prevalence of type 1 Brugada pattern from 12pm-6pm & unmasking by fast and a large meal, showing influence by glucose intake and insulin levels. 

 

 

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Not So Benign: Benign early repolarization (BER) effects in STEMI

- Benign early repolarization (BER) has been associated with increased risk of sudden cardiac death and ventricular fibrillation (VF) in patients with and without structural heart disease.

- Acute STEMI is associated with high incidence of ventricular arrhythmias and the most frequent cause of sudden cardiac death in the adult population.

- BER has been associated with arrhythmogenicity, however the prognostic importance of this ECG finding in patients with STEMI has not been well elucidated.

- In a recent prospective study of STEMI patients, BER was associated with higher rates of in-hospital ventricular arrhythmias and mortality; It is an independent predictor of long-term mortality beyond well-known other parameters. 

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Predictors of Cardiac Rupture After AMI

- In the era of revascularization and aggressive cardiac care there has been a continual decline in acute myocardial infarction (AMI) mortality rates; however one of the most deadly complications, cardiac rupture (left ventricular free wall, ventricular septum, or papillary muscle rupture), still remains relatively stable.

- Cardiac rupture is an increasingly more frequent cause of death during AMI, thus a recent study retrospectively assessed the clinical and morphologic variables in those with and without cardiac rupture that were hospitalized for AMI.

- Cardiac rupture overwhelmingly complicates a first AMI.

- Cardiac rupture occurs most often in patients with an immense quantity of cardiac adipose tissue, the size of the left ventricular cavity is typically normal, and the area of the infarct is small.

- Heart failure patients with prior AMI have healed scar tissue and are at nominal risk of complications such as rupture if a subsequent AMI occurs.  

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Title: Patent Foramen Ovale: To Close or Not to Close

Category: Cardiology

Keywords: Patent Foramen Ovale (PubMed Search)

Posted: 11/23/2014 by Semhar Tewelde, MD (Updated: 2/18/2025)
Click here to contact Semhar Tewelde, MD

Patent Foramen Ovale: To Close or Not to Close

- Patent foramen ovale (PFO) is associated with a 3-fold increased risk for recurrent stroke, yet current guidelines only recommends “consideration” of PFO closure after a second cryptogenic stroke.

- Studies have demonstrated reductions in recurrent neurologic events with transcatheter PFO closure compared with medical therapy alone.

- Until recently the cost-effectiveness of PFO closure has not been described.

- Although PFO closure was found to be immediately more costly per patient closure, it reached cost-effectiveness at ~2.5 years of follow-up.

- Closure of PFO is both beneficial in terms of risk-benefit and cost-effectiveness strategy, especially as cryptogenic stroke typically affects the young.

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Coronary Subclavian Steal Syndrome

Coronary subclavian steal syndrome (CSSS) is defined as coronary ischemia resulting from the reversal of flow in an internal mammary arterial graft usually secondary to subclavian stenosis.

Angiographic subclavian stenosis is defined as greater than 50% narrowing or greater than 20mmHg pressure difference across a lesion.

CSSS occurs in up to 4.5% of patients with prior CABG & common in older individuals with existing peripheral vascular disease.

CSSS most commonly manifests as stable angina, but frequently presents as unstable angina, acute myocardial infarction, acute systolic heart failure or even cardiogenic shock.

Screening for subclavian stenosis prior to CABG w/bilateral noninvasive blood pressure assessment, and a 15 mmHg or greater discordance should elicit further imaging.

Percutaneous revascularization is the first-line therapy for CSSS and has excellent long-term outcomes. 

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Heart Failure & Pulmonary Hypertension (Part II)

- HFpEF-PH management guidelines recommend the treatment of symptoms of congestion and volume overload, targeting LV relaxation and co-morbidities; including the management of pulmonary congestion, ischemia, sleep apnea, atrial fibrillation, and diabetes.

- Both atrial/ventricular dysrhythmias contribute to the mortality associated with HF & control of particularly atrial fibrillation, is an essential part of the early pulmonary vascular remodeling process.

- Both endothelin receptor antagonists (ERA) and prostanoids have been effective for PAH & clinical trials utilizing these agents have also been attempted in treatment of PH due to left heart disease, but have proven to be either neutral or even detrimental.

- Selective dilation of the pulmonary vessels in patients with postcapillary PH, without simultaneously ensuring the unloading of the LV, can cause profound pulmonary venous congestion resulting in sudden pulmonary edema, which greatly increases the morbidity in patients with this form of PH.

- Currently, the most compelling published data for pharmacological treatment targeting PH in HFpEF involves phosphodiesterase (PDE) inhibitor sildenafil.

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Heart Failure & Pulmonary Hypertension (Part I)

~50% of patients with heart failure & preserved ejection fraction (HFpEF) develop pulmonary hypertension (PH)

HFpEF with PH portends reduced survival and increased hospitalization rates compared to those without PH

HFpEF-PH is often confused with idiopathic pulmonary hypertension (IPAH) given the similar hemodynamics; differentiating them is challenging and requires careful consideration of clinical, radiologic, and hemodynamic data

 

 

PAH

HFpEF

Clinical parameters:

 Age

Typically 3rd–5th decade

Typically 6th–8th decade

 Comorbidities (HTN, HLD, DM, CAD)

Rare

Common

 Atrial arrhythmias

Rare

Common

 Obstructive sleep apnea

Rare

Common

Echocardiographic parameters:

 LA size/volume

Normal

Increased

 LV diastolic function

Normal to mildly abnormal

Moderate to severely abnormal

Hemodynamic parameters:

 Resting PAWP

Always <15 mmHg

May be < or >15 mmHg

 Response to volume

PAWP <15 mmHg (increase ≤5 mmHg)

PAWP >15 mmHg (increase >5 mmHg)

 Response to exercise

PAWP <15 mmHg (increase ≤5 mmHg)

PAWP >15 mmHg (increase >5 mmHg)

(Table reproduced from article)

 

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Cardiovascular Morbidity & Sleep Apnea

Obstructive sleep apnea (OSA) is characterized by sleep-related periodic breathing, upper-airway obstruction, sleep disruption, and hemodynamic perturbations

Epidemiological data shows a strong association between untreated OSA & cardiovascular morbidity/mortality

Two recent studies by Gottlieb et al. (1) & Chirinos et al. (2) elucidated two important explicit and complicit treatment considerations for OSA

(1) In moderate-to-severe obstructive sleep apnea, the use of CPAP alone during sleep may ameliorate systemic hypertension and cardiovascular risk, even in patients who do not have "subjective" sleepiness

(2) Weight loss combined with CPAP use may further decrease cardiovascular morbidity

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Title: Kounis Syndrome (Part II)

Category: Cardiology

Posted: 10/12/2014 by Semhar Tewelde, MD (Updated: 2/18/2025)
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Kounis Syndrome (Part II)

- KS can develop from multiple etiologies: hymenoptera, proteins, vasoactive amines, histamine, acetylcholine, multiple antibiotics, and various medical conditions (angioedema, serum sickness, asthma, stress-induced cardiomyopathy).

- Hypersensitivity myocarditis and KS are two cardiac entities of allergic etiology affecting the myocardium and coronary arteries, respectively. These two entities can mimic each other and can be clinical indistinguishable.

- Presence of eosinophil’s, atypical lymphocytes, and giant cells on myocardial biopsy suggests hypersensitivity myocarditis.

- There is evidence showing use of corticosteroids with vasospastic angina with evidence of allergy or the presence of symptoms refractory to high-dose vasodilators has been reported to resolve symptoms.

 

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Kounis Syndrome (Part I)

- Kounis & Zavras (1991) described the syndrome of allergic angina and allergic myocardial infarction, currently known as Kounis syndrome (KS). Braunwald (1998) noted vasospastic angina can be induced by allergic reactions, with mediators such as histamine and leukotrienes acting on coronary vascular smooth muscle.

- Two subtypes have been described: type I, occurring in patients without predisposing factors for CAD often caused by coronary artery spasm and type II, occurring with angiographic evidence of coronary disease when the allergic events induce plaque erosion or rupture.

- This syndrome has been reported in association with a variety of medical conditions, environmental exposures, and medication exposures. Entities such as Takotsubo cardiomyopathy, drug-eluted stent thrombosis, and coronary allograft vasculopathy also appear to be associated with this syndrome.

-  Clinical presentation includes: symptoms and signs of an allergic reaction and acute coronary syndrome: chest pain, dyspnea, faintness, nausea, vomiting, syncope, pruritus, urticaria, diaphoresis, pallor, palpitations, hypotension, and bradycardia. 

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Ventricular Arrhythmias Originating from the Moderator Band

- Ventricular arrhythmias originating from the moderator band (MB) often have a distinct morphology

- Typically MB arrhythmias have a left bundle branch block pattern, QRS with a late precordial transition (>V4), a rapid down stroke of the QRS in the precordial leads, and a left superior frontal plane axis

- MB arrhythmias are often associated with PVC-induced ventricular fibrillation

- Catheter ablation is quite effective at termination of the arrhythmias and facilitated with intracardiac echocardiography (ICE)

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Optimal Revascularization in Complex Coronary Artery Disease

- A multicenter trial 4,566 patients with NSTEMI, unstable angina, and multi-vessel coronary artery disease were enrolled comparing outcomes of cardiac stenting versus coronary artery bypass.

- Cardiac stenting was associated with improved outcomes and lower mortality in the following subgroups: age >65 years, women, unstable angina, TIMI score >4, and 2 vessel disease.

- Despite high clinical risk patients who underwent cardiac stenting compared to surgical revascularization did better in this prospective registry. 

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PARADIGM Shift in Heart Failure

- Angiotensin-converting enzymes inhibitors (ACE-I) are cornerstone for treatment of heart failure (HF) given the multiple trials which have shown their positive risk reduction in cardiovascular death.

- Studies looking at the effect of angiotensin-receptor blockers (ARBs) on mortality have been inconsistent; thus ARB's have been recommended as 2nd-line for those who have unacceptable side effects to ACE-I.

- A recent double-blinded RCT (PARADIGM-HF)  ~8400 patients with class II-IV HF w/ ejection fraction <40% were treated with enalapril (standard therapy) versus novel therapy with neprilysin (neutral endopeptidase) inhibitor combined with an ARB.

- Primary outcomes were death from cardiovascular causes and hospitalization for HF; The RCT was ceased early (~27 months) because of an overwhelming benefit with the new agent.

- At study closure death occurred 26.5% in the standard group versus 21.8% in the novel group. The risk of HF hospitalization was decreased 21% with novel therapy.

- In early studies the use of a neprilysin inhibitor combined with an ARB has shown superior effects to current standard therapy (ACE-I), however long-term effects of this novel therapy are yet to be determined. 

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Title: Sick Sinus Syndrome

Category: Cardiology

Keywords: Sick Sinus Syndrome (PubMed Search)

Posted: 8/31/2014 by Semhar Tewelde, MD
Click here to contact Semhar Tewelde, MD

Sick Sinus Syndrome

- Sick sinus syndrome (SSS) is a cardiac conduction disorder characterized by symptomatic dysfunction of the sinoatrial (SA) node.

- SSS usually manifests as sinus bradycardia, sinus arrest, or sinoatrial block, and is sometimes accompanied by supraventricular tachydysrhythmias.

- Symptoms of SSS include: syncope, dizziness, palpitations, exertional dyspnea, fatigability from chronotropic incompetence, heart failure, and angina.

- Clinically significant SSS typically requires pacemaker implantation. Approximately 30% to 50% of pacemaker implantation in the United States list SSS as the primary indication.

- 2 large, prospective cohorts with an average follow-up of 17 years, observed the incidence of SSS increases with age, does not differ between men and women, and is lower among blacks than whites.

- Risk factors for SSS included greater BMI & height, elevated NT-proBNP level & cystatin C level, longer QRS interval, lower heart rate, hypertension, and right bundle branch block.

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Title: GRACE Score

Category: Cardiology

Keywords: GRACE score (PubMed Search)

Posted: 8/24/2014 by Semhar Tewelde, MD (Updated: 2/18/2025)
Click here to contact Semhar Tewelde, MD

GRACE Score  

- The Global Registry of Acute Coronary Events (GRACE) is an international database tracking outcomes of patients presenting with acute coronary syndromes (ACS).

- GRACE score is calculated based on 8 variables: Age, HR, systolic BP, creatinine, killip class, ST-segment deviation on EKG, cardiac biomarkers, and cardiac arrest on admission.

- Several reports have shown that the GRACE score is a better predictor of clinical outcome (risk of death or the combined risk of death or myocardial infarction at 6 months) than the TIMI score.

- A recent study evaluated the relationship between GRACE score & severity of coronary artery disease (CAD) angiographically evaluated by Gensini score in patients with NSTE-MI.

- Results showed that the GRACE score has significant relation with the extent & severity of CAD as assessed by angiographic Gensini score.

- GRACE score was shown to be important both for determining the severity of the CAD and predicting death within 6 months of hospital discharge from NSTE-MI.

 

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